Article Figures & Data
Figures
- Fig. 1.
Effects of starvation and feeding on anandamide levels in the brain and small intestine. Starvation promoted the accumulation of anandamide in the small intestine. Data are the means ± SEM of at least five determinations per group. **p < 0.01, fed versus starved group; Newman–Keuls.
- Fig. 2.
Peripheral effects of cannabinoids on food intake. A, AEA elicited hyperphagia in partially satiated animals when injected after a 60 min meal. B, Anandamide has no effect after intracerebroventricular administration.C, Acute intraperitoneal injection of WIN55,212-2 (WIN) promoted hyperphagia in partially satiated animals. D, WIN55,212-2 had no effect after intracerebroventricular injection. E, Acute intraperitoneal injection of SR141716A (SR) reduced food intake in food-deprived rats during the 240 min testing period.F, The intracerebroventricular administration of SR141716A did not affect food intake in food-deprived animals. Data are means ± SEM of at least 10 determinations per group. *p < 0.01 versus vehicle-treated group (white bars); Newman–Keuls.
- Fig. 3.
A, Capsaicin treatment abolished the anorexic effect of CCK-8, which acts peripherally, but not that of the 5-HT-1B agonist CP93129, which acts centrally.B, WIN55,212-2 (WIN) did not produce hyperphagia in capsaicin-treated rats. C, Capsaicin treatment abolished the reduction of food intake elicited by SR141716A (SR) in food-deprived rats.VEH, Vehicle. Data are the means ± SEM of at least 10 determinations per group. *p < 0.01 versus vehicle-treated group; Newman–Keuls.
- Fig. 4.
A, OEA blocked hyperphagia elicited by AEA (10 mg/kg) when injected 30 min before the endogenous cannabinoid in partially satiated rats. VEH, Vehicle.B, SR141716A (SR) potentiates the feeding suppression induced by OEA. The effects of a subthreshold dose of SR141716A (0.3 mg/kg, i.p.) on OEA (0.5, 1, and 5 mg/kg, i.p.) induced feeding suppression on food intake in 24 hr food-deprived rats 1 hr after the injection of OEA. Either vehicle (open bars) or SR141716A (black bars) was injected 30 min before OEA. Similar results were obtained 4 and 24 hr after the administration of drugs (data not shown). Data are the means ± SEM of at least 10 determinations per group. *p < 0.01 versus vehicle-treated group; Newman–Keuls.#p < 0.01 versus 0 dose.
Tables
- Table 1.
Effects of either central (intracerebroventricular) or peripheral (intraperitoneal) administration of vehicle and the CBl cannabinoid receptor antagonist SR141716A on motor behaviors measured in the open field
Crossings Rearings Time spent grooming Vehicle, (intracerebroventricular) 160.6 ± 20.9 46.0 ± 6.2 27.8 ± 8.5 SR141716A, (5 μg/5 μl, i.c.v.) 120.8 ± 18 20.2 ± 5.9* 84.5 ± 14.5* Vehicle, (intraperitoneal) 143.3 ± 0.7 30.9 ± 4.1 8.8 ± 4.2 SR141716A, (3 mg/kg, i.p.) 156.9 ± 24.7 9.0 ± 2.7* 25.4 ± 10.6* ↵* p < 0.05; Newman–Keuls.
